Despite experimental use of polymorphonuclear granulocyte (PMN) transfusions for nearly 20 years, considerable controversy persists as to their efficacy and to the possible complications of their collection and use. Our experience with PMN dysfunction and pulmonary sequestration in hemodialysis - a type of extracorporeal circulation not unlike that utilized in certain leukapheresis systems - provokes us to investigate the possibility that complement-induced PMN dysfunction may render leukapheresed granulocytes therapeutically impotent. We have accumulated evidence that certain foreign surfaces, including dialyzer cellophane and nylon filters in continuous flow filtration (CFF) leukapheresis apparati, are capable of activating the plasma complement cascade. Certain of these activated components alter the membranes of PMNs, impairing their chemotactic activity, and promoting their adhesion to artificial and to endothelial surfaces. Such adhesion with plugging occurs predominantly in the pulmonary microvasculature of the dialyzed patient and causes significant pulmonary dysfunction. We propose to determine if similar deleterious effects occur in leukapheresis (particulary CFF) donors and recipients. In ancillary studies we shall study whether the acute respiratory distress which occurs in septic patients ("shock lung") and sporadically in leukemic and aplastic anemia patients following bone marrow transplantation involves analogous complement-mediated pulmonary vascular leukostasis.